JID innovations : skin science from molecules to population health最新文献_第10页

Metabolomic and Lipidomic Alterations in Patients with Atopic Dermatitis with Dupilumab-Associated Ocular Surface Disease 杜匹单抗相关眼表疾病的特应性皮炎患者的代谢组学和脂质组学改变

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2025-03-08 DOI: 10.1016/j.xjidi.2025.100361

VijayKumar Patra , Nora Woltsche , Natalie Bordag , Urban Cerpes , Danijela Bokanovic , Maria Repelnig , Yohann Clement , Isabella Perchthaler , Harald Köfeler , Manuela Fischl , Franz Legat , Andreas Wedrich , Jutta Horwath-Winter , Sophie Ayciriex , Peter Wolf

{"title":"Metabolomic and Lipidomic Alterations in Patients with Atopic Dermatitis with Dupilumab-Associated Ocular Surface Disease","authors":"VijayKumar Patra , Nora Woltsche , Natalie Bordag , Urban Cerpes , Danijela Bokanovic , Maria Repelnig , Yohann Clement , Isabella Perchthaler , Harald Köfeler , Manuela Fischl , Franz Legat , Andreas Wedrich , Jutta Horwath-Winter , Sophie Ayciriex , Peter Wolf","doi":"10.1016/j.xjidi.2025.100361","DOIUrl":"10.1016/j.xjidi.2025.100361","url":null,"abstract":"<div><div>Atopic dermatitis (AD) is an inflammatory skin disease characterized by chronic pruritic eczema with an estimated prevalence of 10% in adults and 50% of them suffering from moderate-to-severe manifestations. Dupilumab, an IL-4/IL-13 inhibitor, is approved for treating moderate-to-severe AD. However, dupilumab-associated ocular surface disease (DAOSD) emerges in up to 60% of dupilumab-treated patients, constituting a major AD-specific adverse event. DAOSD pathogenesis has not been fully understood yet. To elucidate the metabolic changes occurring after dupilumab treatment in patients with AD, we focused in this prospective single-center cohort study particularly on patients who developed DAOSD. In total, 20 patients with AD underwent dupilumab therapy, with 6 developing DAOSD. Plasma and serum samples were collected at baseline, 4 and 16 weeks after treatment initiation, and during the conjunctivitis episode. In addition, 10 age- and sex-matched healthy controls were sampled solely at baseline. High-resolution mass spectrometry was employed for metabolomic and lipidomic analysis of all blood samples. Targeted metabolomics and lipidomic with multivariate analysis unveiled significant metabolic and lipidic disparities (such as increased activity of benzoic acid, tyrosine and indole metabolism, and others) between AD patients with and those without DAOSD. Metabolomics and lipidomic analysis further deepen our comprehension of DAOSD pathogenesis.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100361"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity 化脓性隧道汗腺炎：揭示一种独特的疾病实体

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2025-01-21 DOI: 10.1016/j.xjidi.2025.100350

Nicole Vecin , Nathan C. Balukoff , Marita Yaghi , Tammy Gonzalez , Andrew P. Sawaya , Natasa Strbo , Marjana Tomic-Canic , Hadar Lev-Tov , Irena Pastar

{"title":"Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity","authors":"Nicole Vecin , Nathan C. Balukoff , Marita Yaghi , Tammy Gonzalez , Andrew P. Sawaya , Natasa Strbo , Marjana Tomic-Canic , Hadar Lev-Tov , Irena Pastar","doi":"10.1016/j.xjidi.2025.100350","DOIUrl":"10.1016/j.xjidi.2025.100350","url":null,"abstract":"<div><div>Hidradenitis suppurativa tunnel structures lined with epithelium within the dermis are unique features of advanced disease stages that significantly impair patients’ QOL. The presence of hidradenitis suppurativa tunnels is associated with a decreased likelihood of achieving a clinical response, even when receiving biological therapy. The cellular and molecular mechanisms underlying tunnel formation and pathology are only partially understood, which hampers the development of more effective targeted therapies. Tunnels create a unique microenvironment that drives a vicious cycle of hidradenitis suppurativa inflammation, with tunnel keratinocytes exhibiting an activated phenotype characterized by distinct gene expression signatures. In this review, we summarize the current literature and discuss aspects of the pathophysiology of tunnels, including the role of hair follicle epidermal stem cells in tunnel formation, potential role of fibroblast-mediated epithelial–mesenchymal transition, role of dermal papilla fibroblasts, and aberrant proinflammatory repair response contributing to the observed fibrosis and scarring. Finally, tunnel structures are characterized by unique microbial dysbiosis and an overabundance of Gram-negative anaerobes that are not targeted by current therapeutics. In addition to outlining the possible mechanisms of tunnel formation, we provide perspectives on the translation of current knowledge into more effective treatment approaches for patients with hidradenitis suppurativa tunnels.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100350"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Impact of Air Pollution on Disease Activity in Bullous Pemphigoid and Pemphigus 空气污染对大疱性类天疱疮和天疱疮疾病活动性的影响。

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2024-11-29 DOI: 10.1016/j.xjidi.2024.100334

Ron Feldman , Emily F. Cole

{"title":"The Impact of Air Pollution on Disease Activity in Bullous Pemphigoid and Pemphigus","authors":"Ron Feldman , Emily F. Cole","doi":"10.1016/j.xjidi.2024.100334","DOIUrl":"10.1016/j.xjidi.2024.100334","url":null,"abstract":"<div><div>With a growing awareness of climate change, air pollution has emerged as an important contributor to the development and exacerbation of inflammatory skin conditions. However, the effect of air pollution on immunobullous disease activity is unknown. In this study, we performed a retrospective cohort study of 115 patients with bullous pemphigoid and 152 patients with pemphigus from a university-based specialty clinic in the Southeastern United States. We compared standardized disease activity measures with inhalable particulate matter (particulate matter ≤2.5, particulate matter ≤10), ozone, atmospheric pollutants (sulphur dioxide, carbon monoxide, nitrogen dioxide), and air quality index. Results demonstrated small but statistically significant associations between Bullous Pemphigoid Disease Area Index total activity score and several variables (particulate matter ≤2.5, sulphur dioxide, and air quality index). In addition, there were small but significant negative correlations between ozone and bullous pemphigoid disease area index pruritus score as well as carbon monoxide and pemphigus disease area index score. This study suggests that air pollution may impact disease activity in bullous pemphigoid to a greater extent than pemphigus. Future studies should be aimed at identifying potential mechanisms for this association.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100334"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143082589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Meeting Report on “The International Congress on Autoimmune Pre-disease (2024)” “自身免疫性疾病前期国际大会（2024）”会议报告

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2024-12-18 DOI: 10.1016/j.xjidi.2024.100342

Justus Ohmes , Afsaneh Mehrpouyan , Julia Wimmer-Groß , Abdul Razzaque Ahmed , Kyle T. Amber , Swayanka Biswas , Angela Christiano , Shirin Emtenani , Stephanie Goletz , Jennifer Elisabeth Hundt , Laura Kirchhoff , Khalaf Kridin , Julie Lasselin , Matthias Laudes , Wing Yu Lee , Ralf J. Ludwig , Sripriya Murthy , Sadegh Mousavi , Tamas Nemeth , Mareike Neumann , Sarah Stenger

引用次数: 0

The Volume-Regulated Anion Channel LRRC8 is Involved in the Initiation of Epidermal Differentiation and is Deregulated in Psoriasis 体积调节阴离子通道LRRC8参与表皮分化的启动，并在银屑病中失调

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2025-02-17 DOI: 10.1016/j.xjidi.2025.100357

Magdalena Jahn , Victoria Lang , Oliver Rauh , Torsten Fauth , Claudia Buerger

{"title":"The Volume-Regulated Anion Channel LRRC8 is Involved in the Initiation of Epidermal Differentiation and is Deregulated in Psoriasis","authors":"Magdalena Jahn , Victoria Lang , Oliver Rauh , Torsten Fauth , Claudia Buerger","doi":"10.1016/j.xjidi.2025.100357","DOIUrl":"10.1016/j.xjidi.2025.100357","url":null,"abstract":"<div><div>Recent studies have shown that LRRC8A, the essential subunit of the volume-regulated anion channel LRRC8, which is responsible for mediating cell volume regulation during hypotonic stress, is predominantly localized in the basal layer of the epidermis. This prompted us to investigate whether LRRC8A plays a role in maintaining epidermal homeostasis by regulating key processes initiated in this layer, such as cell proliferation and/or differentiation.</div><div>LRRC8A was found to be strongly upregulated in transiently amplifying cells at the onset of differentiation. While <em>LRRC8A</em> mRNA remains high when keratinocytes mature further, the LRRC8A protein is drastically downregulated. Interference with <em>LRRC8A</em> expression at this step inhibits the transition of keratinocyte stem cells into transiently amplifying cells and impairs terminal differentiation. As psoriasis is a common chronic inflammatory skin disease characterized by disturbed epidermal differentiation and aberrant function of transiently amplifying cells, we investigated the involvement of LRRC8A in this disease. Indeed, LRRC8A was strongly decreased in lesional psoriatic skin, which could also be mimicked in vitro using Th1/Th17 cytokine mixes. Thus, our data suggest that LRRC8 could serve as a therapeutic target for the topical treatment strategies of psoriatic lesions by restoring the capacity of keratinocytes to initiate differentiation.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100357"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Meeting Report on “10th Anniversary Symposium on Inflammatory Skin Disease” “炎症性皮肤病十周年研讨会”会议报告

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2024-12-24 DOI: 10.1016/j.xjidi.2024.100344

Shirin Emtenani , John F. Baines , Katja Bieber , Evelyn Gaffal , Stephanie Goletz , Gema Hernández , Misa Hirose , Markus Hoffmann , Pascal Joly , Henriette Kirchner , Jörg Köhl , Sripriya Murthy , Sabrina Patzelt , Frank Petersen , Manuela Pigors , Gabriela Riemekasten , Leon F. Schmidt-Jiménez , Tanya Sezin , Malte Spielmann , Diamant Thaçi , Enno Schmidt

引用次数: 0

Efficient Dual Cas9 Nickase Correction of a Prevalent Pathogenic LAMB3 Variant for Junctional Epidermolysis Bullosa 结性大疱性表皮松解症常见致病性LAMB3变异的有效双Cas9缺失酶校正

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2024-12-24 DOI: 10.1016/j.xjidi.2024.100343

Alex du Rand , John Hunt , Daniel Verdon , Ben Buttle , P. Rod Dunbar , Diana Purvis , Vaughan Feisst , Hilary Sheppard

{"title":"Efficient Dual Cas9 Nickase Correction of a Prevalent Pathogenic LAMB3 Variant for Junctional Epidermolysis Bullosa","authors":"Alex du Rand , John Hunt , Daniel Verdon , Ben Buttle , P. Rod Dunbar , Diana Purvis , Vaughan Feisst , Hilary Sheppard","doi":"10.1016/j.xjidi.2024.100343","DOIUrl":"10.1016/j.xjidi.2024.100343","url":null,"abstract":"<div><div>Gene editing facilitated by homology-directed repair represents a promising strategy for precisely correcting pathogenic variants underlying monogenic disorders, including the life-threatening skin blistering condition junctional epidermolysis bullosa (JEB). Frequent reports of unintended off-target genotoxicity associated with conventional Cas9 nuclease editing have increasingly led to the adoption of dual-Cas9 nickases (dual-Cas9n) owing to their improved safety profile. However, rates of precise repair obtained with such strategies remain low. In this study, we establish a dual-Cas9n approach targeting <em>LAMB3</em>, using electroporation to deliver Cas9-nickase ribonucleoproteins and modified single-stranded oligodeoxynucleotide repair templates into primary JEB keratinocytes. Targeting a hotspot pathogenic variant (c.1903C>T, p.R635∗), we report perfect correction efficiencies of up to 54% based on standard next-generation sequencing. Using a high-fidelity Cas9 nuclease, we also report perfect repair of up to 74% when using a small-molecule modulator of DNA repair. Dual-Cas9n–corrected JEB keratinocytes demonstrated restored laminin-332 expression and secretion <em>in vitro</em>, leading to improved cellular adhesion and accurate laminin-332 localization in engineered skin equivalents. This protocol represents a significant improvement in precision gene repair using Cas9 nickases for epidermolysis bullosa, with the potential to be applied to a large cohort of patients harboring this prevalent pathogenic variant.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100343"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143101038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Carvedilol Prevents UV-Induced Immunosuppression and Skin Carcinogenesis through a Mechanism Independent of β-Blockade 卡维地洛通过独立于β-受体阻滞剂的机制防止紫外线诱导的免疫抑制和皮肤癌发生

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2025-03-24 DOI: 10.1016/j.xjidi.2025.100365

Ayaz Shahid , Fanglong Dong , Bradley T. Andresen , Ying Huang

{"title":"Carvedilol Prevents UV-Induced Immunosuppression and Skin Carcinogenesis through a Mechanism Independent of β-Blockade","authors":"Ayaz Shahid , Fanglong Dong , Bradley T. Andresen , Ying Huang","doi":"10.1016/j.xjidi.2025.100365","DOIUrl":"10.1016/j.xjidi.2025.100365","url":null,"abstract":"<div><div>Exposure to UVR suppresses the immune system, which plays a primary role in skin cancer etiology. The β-blocker carvedilol prevents UV-induced skin cancer, but the mechanism is unknown. This study examined the effects of carvedilol and its enantiomers on UV-induced immunosuppression using contact hypersensitivity (CHS) response in SKH-1 mice. A single-dose UVR (224 mJ/cm<sup>2</sup>) strongly suppressed CHS, which was attenuated by intraperitoneal injection of carvedilol before UV exposure. Adoptive transfer of lymphocytes isolated from UV-irradiated mice to naïve mice without UV exposure triggered CHS suppression, which was not observed for lymphocytes isolated from carvedilol-treated mice. Topically applied carvedilol also prevented UV-induced CHS suppression. Both the β-blocking S-carvedilol and non–β-blocking R-carvedilol attenuated UV-induced CHS suppression. To evaluate the role of β2-adrenergic receptor, a knockout mouse model of β2-adrenergic receptor on the SKH-1 background was used. UV suppressed CHS in β2-adrenergic receptor–knockout mice, and carvedilol attenuated UV-induced CHS suppression in both genotypes. Furthermore, wild-type and knockout mice exposed to chronic UVR developed skin tumors with similar incidence, multiplicity, and tumor burden, whereas carvedilol inhibited skin tumor development in both genotypes. These data suggest that carvedilol prevents skin cancer not through β-blocking but through its activity overcoming UV-induced immunosuppression.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100365"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143816506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Machine Learning for Early Detection of Hidradenitis Suppurativa: A Feasibility Study Using Medical Insurance Claims Data 机器学习用于化脓性汗腺的早期检测：使用医疗保险索赔数据的可行性研究

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2025-03-10 DOI: 10.1016/j.xjidi.2025.100362

Waqar Ali , Jonathan Williams , Betty Xiong , James Zou , Roxana Daneshjou

{"title":"Machine Learning for Early Detection of Hidradenitis Suppurativa: A Feasibility Study Using Medical Insurance Claims Data","authors":"Waqar Ali , Jonathan Williams , Betty Xiong , James Zou , Roxana Daneshjou","doi":"10.1016/j.xjidi.2025.100362","DOIUrl":"10.1016/j.xjidi.2025.100362","url":null,"abstract":"<div><div>Patients with hidradenitis suppurativa (HS) are often misdiagnosed and may wait up to 10 years to receive a diagnosis of HS. This study aimed to predict HS diagnosis prior to actual diagnosis on the basis of previous medical history using models developed with insurance claims data. Three machine learning models were compared with a model using features selected by a dermatologist (clinical baseline model). The study analyzed 5,900,000 United States individuals’ insurance records over 13.5 years. The population included 13,886 patients with HS with at least 1 claim in each of the 2 years prior to their first HS diagnosis and 69,428 control patients with no HS diagnosis. The models aimed to classify HS diagnosis status on the basis of clinical features observed over 2 years. Model performance was assessed by area under the receiver operating characterisitic curve, F1-score, and precision and recall rates. The machine learning models (logistic regression, random forest, and XGBoost) showed a higher area under the receiver operating characterisitic curve than the clinical baseline model (logistic regression = 0.75, random forest = 0.79, XGBoost = 0.80, clinical = 0.71). In the clinical model and the best-performing XGBoost model, the top features associated with diagnosis were patient age at prediction and sex. The XGBoost model top features also included the use of sulfamethoxazole/trimethoprim and clindamycin phosphate and obesity.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100362"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lack of Hypoxia Inducible Factor-1α Influences on Macrophages Ability to Deal with Leishmania braziliensis In Vitro and Affects Pathology In Vivo 缺乏缺氧诱导因子-1α对巨噬细胞体外处理巴西利什曼原虫能力的影响及体内病理

JID innovations : skin science from molecules to population health Pub Date : 2025-05-01 Epub Date: 2025-01-08 DOI: 10.1016/j.xjidi.2025.100347

Rodrigo C.O. Sanches , Leonardo G. Vaz , Fabio V. Marinho , Erika S. Guimarães , Edgar M. Carvalho , Lucas P. Carvalho , Sergio C. Oliveira

{"title":"Lack of Hypoxia Inducible Factor-1α Influences on Macrophages Ability to Deal with Leishmania braziliensis In Vitro and Affects Pathology In Vivo","authors":"Rodrigo C.O. Sanches , Leonardo G. Vaz , Fabio V. Marinho , Erika S. Guimarães , Edgar M. Carvalho , Lucas P. Carvalho , Sergio C. Oliveira","doi":"10.1016/j.xjidi.2025.100347","DOIUrl":"10.1016/j.xjidi.2025.100347","url":null,"abstract":"<div><div>Cutaneous leishmaniasis, caused by <em>Leishmania braziliensis</em>, still represents a serious health problem in Brazil, especially in the northeast region. Currently, to our knowledge, no report describes the role of hypoxia inducible factor-1α (HIF-1α) during <em>L braziliensis</em> infection. In this study, we demonstrated that the parasite induces HIF-1α expression and stabilization in bone marrow–derived macrophages only when added with exogenous IFN-γ plus lipopolysaccharide. Coherently, we did not find an enrichment in the glycolytic pathway upon bone marrow–derived macrophage infection. Evaluating the impact of HIF-1α absence during macrophage infection in vitro, we observed HIF-1α–knockout cells present at high levels of IL-10, reduced production of nitric oxide, and decreased expression of VEGF-A. As a result, parasite viability improves within HIF-1α–knockout cells. However, in vivo, the absence of myeloid cells expressing HIF-1α had no influence on nitric oxide at tissue levels and in parasite burden. Conversely, lack of HIF-1α significantly affects <em>L braziliensis</em>–induced pathology. Ear lesions induced in myeloid HIF-1α–knockout mice were thicker, presenting higher frequency of macrophages, neutrophils, CD4<sup>+</sup>, and CD8<sup>+</sup> T cells as well as higher levels of IL-12, IL-1β, and IFN-γ, compared with those in wild-type mice. Moreover, draining lymph nodes from myeloid HIF-1α–knockout mice also harbored increased populations of T cells. Our data demonstrate that HIF-1α plays an important role during <em>L braziliensis</em> infection influencing skin pathology in vivo.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100347"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143199481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0